PATHOPHYSIOLOGY

Non-modifiable Age: 0-5 yrs old their immune system is still immature Modifiable Underlying disease condition

Microorganism enters the nose (nasal passages)

Passes through the larynx, pharynx, trachea Microorganism enters lung parenchyma

Passes through the larynx, pharynx, trachea Microorganism enters lung parenchyma

Cough

Activation of Immune response (mucus production) inflamation vasodilation leukocyte and macrophage

Fever

Bacteria multiplies in the alveoli Release of endotoxins and exotoxins from the bacteria (toxins are directly causing the damage to the tissues) Antibiotic: Ampicillin 200mg IVTT Q6 NST 1

Continuous mucus production Narrowing of air passage

Lung consolidation (region of lung tissue filled with liquid) due to cellular exudates (fluid, pus, and blood) from inflammation

Difficulty of breathing

Impaired 02 and C02 exchange due to lung consolidation

Increased respiratory rate

Increase oxygen demand O2 administration Hypoxia Increased pulse rate

Necrosis of pulmonary tissue

Failure of immune response in the pulmonary tissues

The bacterium goes with the blood and release toxins

Whole-body inflammatory state

Inflammatory response Neutrophils marks the pathogen as foreign then signals phagocytes for ingestion of bacteria

Systemic Reaction

Pro-Inflammatory Response (Cytokines)

Anti-Inflammatory Response Interleukin 10 (IL-10) and anti-inflammatory cytokine

Failure of Whole-body inflammatory state

Antibiotic: Ampicillin 200mg IVTT Q6 NST Metronidazole 45mg IVTT

Systemic Infection

(Septicemia)

Body compensates from systemic inflammatory response by slowing things down in order for body to recover.

Decrease systemic vascular resistance

Hypometabolism

Warm, bounding pulses, with brisk capillary refill, edema Antibiotic: Ampicillin 200mg IVTT Q6 NST Metronidazole 45mg IVTT Late Phase

Decreased energy expenditure

Decrease o2 consumption

Vasoconstriction

Cool extremities, poor peripheral pulses

Hyperdrive (Compensatory mechanism) (If the body doesnt recover it goes into hyperdrive) This is partly due to the Exaggerated inflammatory response End of compensatory mechanism (negative feedback mechanism)

Compensatory mechanism: Increase PR Increase RR Increase TEMP

Negative Feedback: diminished PR decrease body TEMP

Poor perfusion Lactic acidosis

Inadequate 02 delivery and nutrients to tissues

Metabolic acidosis Fluid Replacement therapy Medication: Ranitidine 3mg IV Shock or septic shock

MODS Multiple Organ Dysfunction Syndrome due to inability to maintain homeostasis

Hepatic dysfunction

Acute renal failure

Impaired pulmonary function

Disseminated intravascular coagulation (DIC) -also known as consumptive coagulopathy a pathological activation of coagulation (blood clotting) mechanisms

Hyperbilirubinemia

Droplight

DEATH, if not managed.

LEGEND
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